Granuloma: A relatively small nodular inflammatory lesion containing grouped mononuclear phagocytes, caused by infectious and noninfectious agents.Granuloma, Foreign-Body: Histiocytic, inflammatory response to a foreign body. It consists of modified macrophages with multinucleated giant cells, in this case foreign-body giant cells (GIANT CELLS, FOREIGN-BODY), usually surrounded by lymphocytes.Granuloma, Pyogenic: A disorder of the skin, the oral mucosa, and the gingiva, that usually presents as a solitary polypoid capillary hemangioma often resulting from trauma. It is manifested as an inflammatory response with similar characteristics to those of a granuloma.Eosinophilic Granuloma: The most benign and common form of Langerhans-cell histiocytosis which involves localized nodular lesions predominantly of the bones but also of the gastric mucosa, small intestine, lungs, or skin, with infiltration by EOSINOPHILS.Granuloma, Respiratory Tract: Granulomatous disorders affecting one or more sites in the respiratory tract.Granuloma Annulare: Benign granulomatous disease of unknown etiology characterized by a ring of localized or disseminated papules or nodules on the skin and palisading histiocytes surrounding necrobiotic tissue resulting from altered collagen structures.Granuloma, Giant Cell: A non-neoplastic inflammatory lesion, usually of the jaw or gingiva, containing large, multinucleated cells. It includes reparative giant cell granuloma. Peripheral giant cell granuloma refers to the gingiva (giant cell epulis); central refers to the jaw.Granuloma Inguinale: Anogenital ulcers caused by Calymmatobacterium granulomatis as distinguished from lymphogranuloma inguinale (see LYMPHOGRANULOMA VENEREUM) caused by CHLAMYDIA TRACHOMATIS. Diagnosis is made by demonstration of typical intracellular Donovan bodies in crushed-tissue smears.Periapical Granuloma: Chronic nonsuppurative inflammation of periapical tissue resulting from irritation following pulp disease or endodontic treatment.Granuloma, Laryngeal: A tumor-like nodule or mass of inflammatory granulation tissue projecting into the lumen of the LARYNX.Liver Diseases, Parasitic: Liver diseases caused by infections with PARASITES, such as tapeworms (CESTODA) and flukes (TREMATODA).Schistosomiasis mansoni: Schistosomiasis caused by Schistosoma mansoni. It is endemic in Africa, the Middle East, South America, and the Caribbean and affects mainly the bowel, spleen, and liver.Tuberculoma: A tumor-like mass resulting from the enlargement of a tuberculous lesion.Schistosoma mansoni: A species of trematode blood flukes of the family Schistosomatidae. It is common in the Nile delta. The intermediate host is the planorbid snail. This parasite causes schistosomiasis mansoni and intestinal bilharziasis.Sarcoidosis: An idiopathic systemic inflammatory granulomatous disorder comprised of epithelioid and multinucleated giant cells with little necrosis. It usually invades the lungs with fibrosis and may also involve lymph nodes, skin, liver, spleen, eyes, phalangeal bones, and parotid glands.Mycobacterium marinum: A moderate-growing, photochromogenic species found in aquariums, diseased fish, and swimming pools. It is the cause of cutaneous lesions and granulomas (swimming pool granuloma) in humans. (Dorland, 28th ed)Sarcoidosis, Pulmonary: Sarcoidosis affecting predominantly the lungs, the site most frequently involved and most commonly causing morbidity and mortality in sarcoidosis. Pulmonary sarcoidosis is characterized by sharply circumscribed granulomas in the alveolar, bronchial, and vascular walls, composed of tightly packed cells derived from the mononuclear phagocyte system. The clinical symptoms when present are dyspnea upon exertion, nonproductive cough, and wheezing. (Cecil Textbook of Medicine, 19th ed, p431)Lung Diseases, Parasitic: Infections of the lungs with parasites, most commonly by parasitic worms (HELMINTHS).Schistosomiasis: Infection with flukes (trematodes) of the genus SCHISTOSOMA. Three species produce the most frequent clinical diseases: SCHISTOSOMA HAEMATOBIUM (endemic in Africa and the Middle East), SCHISTOSOMA MANSONI (in Egypt, northern and southern Africa, some West Indies islands, northern 2/3 of South America), and SCHISTOSOMA JAPONICUM (in Japan, China, the Philippines, Celebes, Thailand, Laos). S. mansoni is often seen in Puerto Ricans living in the United States.Granuloma, Plasma Cell: A slow-growing benign pseudotumor in which plasma cells greatly outnumber the inflammatory cells.Plasma Cell Granuloma, Pulmonary: A tumor-like inflammatory lesion of the lung that is composed of PLASMA CELLS and fibrous tissue. It is also known as an inflammatory pseudotumor, often with calcification and measuring between 2 and 5 cm in diameter.Epithelioid Cells: Characteristic cells of granulomatous hypersensitivity. They appear as large, flattened cells with increased endoplasmic reticulum. They are believed to be activated macrophages that have differentiated as a result of prolonged antigenic stimulation. Further differentiation or fusion of epithelioid cells is thought to produce multinucleated giant cells (GIANT CELLS).Granuloma, Lethal Midline: A condition that is characterized by inflammation, ulceration, and perforation of the nose and the PALATE with progressive destruction of midline facial structures. This syndrome can be manifested in several diseases including the nasal type of EXTRANODAL NK-T-CELL LYMPHOMA and GRANULOMATOSIS WITH POLYANGIITIS.Gingival DiseasesLung Diseases: Pathological processes involving any part of the LUNG.Mycobacterium bovis: The bovine variety of the tubercle bacillus. It is called also Mycobacterium tuberculosis var. bovis.Ovum: A mature haploid female germ cell extruded from the OVARY at OVULATION.Foreign-Body Reaction: Chronic inflammation and granuloma formation around irritating foreign bodies.Mycobacterium tuberculosis: A species of gram-positive, aerobic bacteria that produces TUBERCULOSIS in humans, other primates, CATTLE; DOGS; and some other animals which have contact with humans. Growth tends to be in serpentine, cordlike masses in which the bacilli show a parallel orientation.Tuberculosis, Hepatic: Infection of the LIVER with species of MYCOBACTERIUM, most often MYCOBACTERIUM TUBERCULOSIS. It is characterized by localized small tuberculous miliary lesions or tumor-like mass (TUBERCULOMA), and abnormalities in liver function tests.Mycobacterium Infections: Infections with bacteria of the genus MYCOBACTERIUM.Lung: Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.Antigens, Helminth: Any part or derivative of a helminth that elicits an immune reaction. The most commonly seen helminth antigens are those of the schistosomes.Cord Factors: Toxic glycolipids composed of trehalose dimycolate derivatives. They are produced by MYCOBACTERIUM TUBERCULOSIS and other species of MYCOBACTERIUM. They induce cellular dysfunction in animals.Mice, Inbred CBACalymmatobacterium: A genus of bacteria causing GRANULOMA INGUINALE and other granulomatous lesions.Skin DiseasesTuberculosis: Any of the infectious diseases of man and other animals caused by species of MYCOBACTERIUM.Schistosoma: A genus of trematode flukes belonging to the family Schistosomatidae. There are over a dozen species. These parasites are found in man and other mammals. Snails are the intermediate hosts.Facial DermatosesLiver Diseases: Pathological processes of the LIVER.Neurocysticercosis: Infection of the brain, spinal cord, or perimeningeal structures with the larval forms of the genus TAENIA (primarily T. solium in humans). Lesions formed by the organism are referred to as cysticerci. The infection may be subacute or chronic, and the severity of symptoms depends on the severity of the host immune response and the location and number of lesions. SEIZURES represent the most common clinical manifestation although focal neurologic deficits may occur. (From Joynt, Clinical Neurology, 1998, Ch27, pp46-50)Macrophages: The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)Tuberculosis, Pulmonary: MYCOBACTERIUM infections of the lung.Mycobacterium avium: A bacterium causing tuberculosis in domestic fowl and other birds. In pigs, it may cause localized and sometimes disseminated disease. The organism occurs occasionally in sheep and cattle. It should be distinguished from the M. avium complex, which infects primarily humans.Schistosomiasis japonica: Schistosomiasis caused by Schistosoma japonicum. It is endemic in the Far East and affects the bowel, liver, and spleen.Petrous Bone: The dense rock-like part of temporal bone that contains the INNER EAR. Petrous bone is located at the base of the skull. Sometimes it is combined with the MASTOID PROCESS and called petromastoid part of temporal bone.Tuberculosis, Lymph Node: Infection of the lymph nodes by tuberculosis. Tuberculous infection of the cervical lymph nodes is scrofula.Mycobacterium Infections, Nontuberculous: Infections with nontuberculous mycobacteria (atypical mycobacteria): M. kansasii, M. marinum, M. scrofulaceum, M. flavescens, M. gordonae, M. obuense, M. gilvum, M. duvali, M. szulgai, M. intracellulare (see MYCOBACTERIUM AVIUM COMPLEX;), M. xenopi (littorale), M. ulcerans, M. buruli, M. terrae, M. fortuitum (minetti, giae), M. chelonae.Mice, Inbred C57BLBiopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Schistosoma japonicum: A species of trematode blood flukes belonging to the family Schistosomatidae whose distribution is confined to areas of the Far East. The intermediate host is a snail. It occurs in man and other mammals.Tuberculosis, Cutaneous: Tuberculosis of the skin. It includes scrofuloderma and tuberculid, but not LUPUS VULGARIS.Splenic DiseasesInterferon-gamma: The major interferon produced by mitogenically or antigenically stimulated LYMPHOCYTES. It is structurally different from TYPE I INTERFERON and its major activity is immunoregulation. It has been implicated in the expression of CLASS II HISTOCOMPATIBILITY ANTIGENS in cells that do not normally produce them, leading to AUTOIMMUNE DISEASES.Lip Diseases

Systemic infection with Alaria americana (Trematoda). (1/1842)

Alaria americana is a trematode, the adult of which is found in mammalian carnivores. The first case of disseminated human infection by the mesocercarial stage of this worm occurred in a 24-year-old man. The infection possibly was acquired by the eating of inadequately cooked frogs, which are intermediate hosts of the worm. The diagnosis was made during life by lung biopsy and confirmed at autopsy. The mesocercariae were present in the stomach wall, lymph nodes, liver, myocardium, pancreas and surrounding adipose tissue, spleen, kidney, lungs, brain and spinal cord. There was no host reaction to the parasites. Granulomas were present in the stomach wall, lymph nodes and liver, but the worms were not identified in them. Hypersensitivity vasculitis and a bleeding diathesis due to disseminated intravascular coagulation and a circulating anticoagulant caused his death 8 days after the onset of his illness.  (+info)

Enhanced Th1 and dampened Th2 responses synergize to inhibit acute granulomatous and fibrotic responses in murine schistosomiasis mansoni. (2/1842)

In murine schistosomiasis mansoni, CD4(+) Th1 and Th2 cells participate in the ovum-induced granulomatous inflammation. Previous studies showed that the interleukin-12 (IL-12)-induced Th1 response strongly suppressed the Th2-cell-mediated pulmonary granuloma development in naive or primed mice. However, liver granulomas were only moderately suppressed in egg-vaccinated, recombinant IL-12 (rIL-12)-treated infected mice. The present study shows that repeated rIL-12 injections given during early granuloma development at 5 to 7 weeks after infection prolonged the Th1 phase and resulted in gamma interferon-mediated suppression of liver granulomas. The timing is crucial: if given at 6 to 8 weeks, during the Th2-dominated phase of florid granuloma growth, the treatment is ineffective. Daily injections of rIL-12 given between 5 and 7.5 weeks during the period of granuloma growth achieved a somewhat-stronger diminution in granuloma growth with less deposition of collagen but caused 60% mortality and liver pathology. In contrast, combined treatment with rIL-12 and anti-IL-4-anti-IL-10 monoclonal antibody (MAb) injections given during the Th2 phase strongly inhibited liver granuloma growth without mortality. The diminished inflammatory response was accompanied by less deposition of collagen in the liver. Moreover, neutralization of endogenous IL-12 by anti-IL-12 MAbs effectively decreased the early Th1 phase (between 5 and 6 weeks after infection) but not the developing Th2 phase (5 to 7 weeks) of granuloma development. These studies indicate that the granulomatous response in infected mice can be manipulated by utilizing the Th1-Th2-subset antagonism with potential salutary results in the amelioration of fibrous pathology.  (+info)

N,N'-Diacetyl-L-cystine-the disulfide dimer of N-acetylcysteine-is a potent modulator of contact sensitivity/delayed type hypersensitivity reactions in rodents. (3/1842)

Oral N-acetyl-L-cysteine (NAC) is used clinically for treatment of chronic obstructive pulmonary disease. NAC is easily oxidized to its disulfide. We show here that N,N'-diacetyl-L-cystine (DiNAC) is a potent modulator of contact sensitivity (CS)/delayed type hypersensitivity (DTH) reactions in rodents. Oral treatment of BALB/c mice with 0.003 to 30 micromol/kg DiNAC leads to enhancement of a CS reaction to oxazolone; DiNAC is 100 to 1000 times more potent than NAC in this respect, indicating that it does not act as a prodrug of NAC. Structure-activity studies suggest that a stereochemically-defined disulfide element is needed for activity. The DiNAC-induced enhancement of the CS reaction is counteracted by simultaneous NAC-treatment; in contrast, the CS reaction is even more enhanced in animals treated with DiNAC together with the glutathione-depleting agent buthionine sulfoximine. These data suggest that DiNAC acts via redox processes. Immunohistochemically, ear specimens from oxazolone-sensitized and -challenged BALB/c mice treated with DiNAC display increased numbers of CD8(+) cells. DiNAC treatment augments the CS reaction also when fluorescein isothiocyanate is used as a sensitizer in BALB/c mice; this is a purported TH2 type of response. However, when dinitrofluorobenzene is used as a sensitizer, inducing a purported TH1 type of response, DiNAC treatment reduces the reaction. Treatment with DiNAC also reduces a DTH footpad-swelling reaction to methylated BSA. Collectively, these data indicate that DiNAC in vivo acts as a potent and effective immunomodulator that can either enhance or reduce the CS or DTH response depending on the experimental conditions.  (+info)

The requirement of an adherent cell substratum for the growth of developing plasmacytoma cells in vivo. (4/1842)

The intraperitoneal injection of pristane (2,6,10,14-tetramethylpentadecane) produces an environment conductive to primary plasmacytoma growth in as few as 3 days. After pristane injection, the total free peritoneal cell population increases from a normal value of 1.55 X 10(6) to 5.28 X 10(6) and remains at this elevated level for at least 50 days. The adherent peritoneal cell population, composed of both mononuclear cells and polymorphonuclear leukocytes, is the primary source of this increase. In the pristane-conditioned peritoneum, these cells rapidly form a chronic granuloma on the peritoneal connective tissues. Daily subcutaneous treatment of mice with 0.5 mg of hydrocortisone beginning simultaneously with pristane injection prevents the increase in the peritoneal cell population, granuloma formation, d the production of a conditoned environment. In mice treated with hydrocortisone beginning 3 days after pristane injection, however, neither the peritoneal cell increase nor the production of a conditioned environment is prevented. The intraperitoneal injection of thioglycolate medium at 4-day intervals produces an elevation of the free adherent peritoneal cell population similar to pristane, but does not produce a granuloma or a conditioned environment. The intraperitoneal transfer of thioglycolate-induced adherent peritonel cells to mice treated with pristane and hydrocortisone simultaneously restores the production of a conditioned environment. These findings indicate that the adherent peritoneal cell population is responsible for the conditioning effect, and that the establishment of a resident population of these cells is necessary to produce conditioning.  (+info)

Experimental murine schistosomiasis in the absence of B7 costimulatory molecules: reversal of elicited T cell cytokine profile and partial inhibition of egg granuloma formation. (5/1842)

The granulomatous inflammation in infection with the helminth Schistosoma mansoni represents a cellular hypersensitivity reaction mediated by, and dependent upon, MHC class II-restricted CD4+ Th cells sensitized to parasite egg Ags. The current work examines the role and significance of the B7:CD28/CTLA-4 pathway in providing the costimulation necessary for the activation of these pathogenic T cells. In vitro T cell responses in B7-1-/- mice, 7-8 wk postinfection, were no different from wild-type controls, but the absence of B7-2 molecules resulted in a decrease in egg Ag-induced proliferation with increased IFN-gamma production. Both B7-1-/- and B7-2-/- mice exhibited intact granuloma formation. In contrast, CD4+ Th cells from B7-1/2 double-deficient mice displayed a dramatic loss of proliferative capacity upon stimulation with egg Ag. Most strikingly, these T cells secreted only IFN-gamma, but not IL-4 and IL-10, a pattern entirely opposite to that displayed by wild-type controls. Despite these major differences in T cell reactivity, B7-1/2-/- mice had only a limited reduction of granuloma size and fibrosis, without appreciable difference in cellular composition. These results show that substantial granuloma formation can occur under conditions of limited T cell expansion and restricted Th1-type cytokine production. They also support the notion that the combined effect of B7 signaling is not as critical for Th1 cell activation as it is for the development of the Th2 dominant environment characteristic of the evolving schistosome infection in H-2b mice.  (+info)

Role of macrophage scavenger receptors in hepatic granuloma formation in mice. (6/1842)

In mice homozygous for the gene mutation for type I and type II macrophage scavenger receptors (MSR-A), MSR-A-/-, the formation of hepatic granulomas caused by a single intravenous injection of heat-killed Corynebacterium parvum was delayed significantly for 10 days after injection, compared with granuloma formation in wild-type (MSR-A+/+) mice. In the early stage of granuloma formation, numbers of macrophages and their precursor cells were significantly reduced in MSR-A-/- mice compared with MSR-A+/+ mice. In contrast to MSR-A+/+ mice, no expression of monocyte chemoattractant protein-1, tumor necrosis factor-alpha, and interferon-gamma mRNA was observed in MSR-A-/- mice by 3 days after injection. Also in MSR-A-/- mice, uptake of C. parvum by Kupffer cells and monocyte-derived macrophages in the early stage of granuloma formation was lower and elimination of C. parvum from the liver was slower than in MSR-A+/+ mice. In the livers of MSR-A+/+ mice, macrophages and sinusoidal endothelial cells possessed MSR-A, but this was not seen in the livers of MSR-A-/- mice. In both MSR-A-/- and MSR-A+/+ mice, expression of other scavenger receptors was demonstrated. These data suggest that MSR-A deficiency impairs the uptake and elimination of C. parvum by macrophages and delays hepatic granuloma formation, particularly in the early stage.  (+info)

The p47(phox-/-) mouse model of chronic granulomatous disease has normal granuloma formation and cytokine responses to Mycobacterium avium and Schistosoma mansoni eggs. (7/1842)

Chronic granulomatous disease (CGD) is a genetic disorder of NADPH oxidase in which phagocytes are defective in generating reactive oxidants. CGD patients suffer from recurrent infections and exuberant and persistent tissue granuloma formation. We hypothesized that abnormal granulomata in CGD may result from aberrant T-cell-mediated cytokine responses. To assess Th-1-type cytokine responses and granulomata, we challenged p47(phox-/-) and wild-type mice with avirulent (SmD) or virulent (SmT) variants of Mycobacterium avium 2-151. To assess Th-2-type cytokine responses and granulomata, we used Schistosoma mansoni eggs (SME). Mononuclear cells were harvested, and cytokine responses were determined by enzyme-linked immunosorbent assay or reverse transcriptase PCR. Following SmD or SmT challenge, splenocytes from p47(phox-/-) and wild-type mice generated similar polar Th-1 responses (increased levels of gamma interferon and basal levels of interleukin 4 [IL-4] and IL-5). By 8 weeks after SmT challenge, exuberant splenic granulomata developed in p47(phox-/-) and wild-type mice. After SME challenge, thoracic lymph node mononuclear cells from p47(phox-/-) and wild-type mice generated similar mixed Th-1 and Th-2 cytokine responses to SME antigen and concanavalin A. Peak lung granuloma sizes and rates of regression were similar in p47(phox-/-) and wild-type mice. These results suggest that exuberant granulomatous inflammation in CGD is probably not the result of skewing of T-cell responses toward the Th-1 or Th-2 pole. Appropriate regression of established tissue granulomata in p47(phox-/-) mice challenged with SME suggests that abnormal granuloma formation in CGD is stimulus dependent and is not an invariant feature of the disease.  (+info)

Sarcoidosis of the upper respiratory tract and its association with lupus pernio. (8/1842)

In a series of 34 patients with sarcoidosis affecting the upper respiratory tract and nose, 26 had lupus pernio (LP) and 17 had sarcoidosis of the upper respiratory tract (SURT). In nine patients these features coexisted. A patient presenting with SURT carried a 50% risk of developing LP although one feature could be present without the other. Both were disorders of women of the child-bearing years of life. SURT, like LP, was an indicator of chronic fibrotic sarcoidosis, developing insidiously and progressing indolently over the years. It was complicated by ulceration, septal perforation, and LP. Three patients had nasal septal perforations, in two instances following submucous resection. This operation is contraindicated in patients with active sarcoidosis, particularly when granulomas are found on nasal biopsy. The Kveim-Siltzbach skin test was positive in all patients with SURT, making it invaluable in the differential diagnosis of granuloma of the nasal cavity.  (+info)

  • Examples of this use of the term granuloma are the lesions known as vocal cord granuloma (known as contact granuloma ), pyogenic granuloma and intubation granuloma, all of which are examples of granulation tissue , not granulomas. (
  • Granuloma gluteale infantum lesions are typically resistant to treatments with barrier creams , antifungal agents , and topical steroids . (
  • On US studies, charcoal granulomas are characterized as irregular-shaped lesions, most often with hyperechogenicity and posterior shadowing. (
  • We report cutaneous granulomas in a child with ataxia telangiectasia AT and compare the clinical course with similar lesions in an adult with common variable immunodeficiency CVI. (
  • In either of these lesions, root canal resection is commonly used, which means that the cyst or granuloma is cleaned by the oral surgery method and the root tip is removed from which the process is started. (
  • Objectives Vocal fold granulomas are benign lesions of the larynx commonly caused by gastroesophageal reflux, intubation, and phonotrauma. (
  • In terms of the underlying cause, the difference between granulomas and other types of inflammation is that granulomas form in response to antigens that are resistant to "first-responder" inflammatory cells such as neutrophils and eosinophils . (
  • Granuloma gluteale infantum may result in post- inflammatory hyperpigmentation and atrophic scarring. (
  • Inflammatory granuloma formation is mediated by TNF-alpha-inducible intercellular adhesion molecule-1. (
  • Recent studies have demonstrated a crucial role for TNF during inflammatory granuloma formation. (
  • Acute schistosomiasis is characterized by pro-inflammatory responses against tissue- or organ-trapped parasite eggs along with granuloma formation. (
  • Consequently, FDG-PET hyperintensity due to charcoal-induced granuloma is very rarely observed, because initial FDG-PET/CT performed just after charcoal subcutaneous injection does not show any early inflammatory reaction, and most often tumor and needle tract are surgically removed before later PET-CT follow-up. (
  • A granuloma is a structure formed during inflammation that is found in many diseases. (
  • However, at longer term, charcoal particles will be ingested and slowly degraded by macrophages, inducing progressive inflammation reaction and, if it remains in situ for more than six months, substantial foreign body granulomas. (
  • Current medical therapy includes inhaled corticosteroids to target inflammation that leads to granuloma formation. (
  • Peripheral giant cell granuloma associated with dental implants: Black female patient, aged 20 years, after 6 months of orthodontic treatment presented to grannuloma private clinic complaining of gingival changes. (
  • Pulmonary hyalinizing granuloma" is a lesion characterized by keloid -like fibrosis in the lung, and is not granulomatous. (
  • We have also assessed the increased expression of ICAM-1, its contribution to granuloma development, and its relationship with TNF during lesion formation. (
  • Increased steady state ICAM-1 mRNA expression was observed in primary egg granulomas when compared with normal lung and foreign body (Sephadex bead) granulomas, which suggests a role for ICAM-1 in Ag-induced lesion formation. (
  • In addition, passive immunization of mice with anti-ICAM-1 mAb during primary granuloma formation resulted in an attenuation of lesion development as compared with lesion development in a control Ab-treated group. (
  • The aim of this case report was to present a clinic case of gravidarum granuloma in the region of lower lingual gingiva, adjacent to an osseointegrated implant in a year-old woman, with 3 months of gestation, who had the lesion since the beginning of her pregnancy. (
  • Mice deficient in Cx3cr1 were protected from granuloma formation and hepatic injury induced by Schistosoma japonicum eggs, as manifested by reduced body weight loss and attenuated hepatomegaly along with preserved liver function. (
  • The antigen causing the formation of a granuloma is most often an infectious pathogen or a substance foreign to the body, but sometimes the offending antigen is unknown (as in sarcoidosis ). (
  • Pulmonary arterial hypertension occurs by two mechanisms in cardiac sarcoidosis: reduced left heart function due to granulomas weakening the heart muscle or from impaired blood flow. (
  • It also frequently causes an increase in 1,dihydroxy vitamin D, the active metabolite of vitamin D , which is usually hydroxylated within the kidney, but in sarcoidosis patients, hydroxylation of vitamin D can occur outside the kidneys, namely inside the immune cells found in the granulomas the condition produces. (
  • On cessation of oral steroids, significant relapse of the facial granuloma occurred. (
  • The most accurate use of the term "granuloma" requires a pathologist to examine surgically removed and specially colored (stained) tissue under a microscope. (
  • A granuloma is a patch of inflamed tissue that has various causes, depending on its location in the body, but is most often caused by a fungal infection, a. (
  • Very occasionally, when a bit of the granuloma detaches (see below), a person may cough up blood or a tiny piece of tissue. (
  • If symptoms at any time during this wait are unacceptable (not usually the case), then the granuloma can be treated with laser ablation in a videoendoscopy laboratory or steroid injection into the abnormal tissue. (
  • Granulomas usually form in reaction to a low-grade, superficial skin infection in periumbilical crevasses and flourish in the moist environment afforded by today's large "super-absorbent" diapers that often cover up the area. (
  • In previous studies using a murine model of filarial infection, granuloma formation was found to be a most important host-protective mechanism. (
  • We recommend the use of broad-spectrum antibiotics in conjunction with systemic steroids for progressive granulomas, as these patients are immunosuppressed and infection with an unidentified organism cannot be excluded. (
  • What causes formation of granuloma? (
  • In the present study, we have examined the mechanism of TNF activation during Schistosoma mansoni egg granuloma formation and its relationship to the expression of ICAM-1. (
  • Our initial studies showed that high affinity human soluble TNFR coupled to the Fc portion of an Ig (sTNFR:Fc construct) could effectively diminish granuloma formation and lymphocyte activation in vivo. (
  • Subsequent studies have demonstrated that sTNFR:Fc treatment down-regulated granuloma formation and ICAM-1 expression, thus suggesting one mechanism of TNF involvement in granuloma formation was through the induction of ICAM-1. (
  • These data demonstrate that both TNF and ICAM-1 participate in lymphocyte activation and granuloma formation and suggest that one mechanism of TNF in granuloma development is through TNF-induced ICAM-1 expression. (
  • We have also shown that in vitro cytoadherence is a surrogate for the formation of antifilarial granulomas in vivo and that it requires "alternatively activated" host cells and a source of antifilarial antibody. (
  • This and other aspects of the kinetics of formation of granulomas have led us to propose that granuloma formation is one, if not the most important, mechanism by which mammals defend themselves against large extracellularly dwelling pathogens. (
  • A mutant mouse strain that has been particularly helpful in dissecting the mechanism of granuloma formation has been the secretory IgM knockout mouse (secIgM −/− mouse) ( 2 , 3 ). (
  • This observation alerted us to the critical role of circulating antifilarial antibodies, particularly of the IgM isotype, in granuloma formation. (
  • In the course of these studies, we found that the adherence of alternatively activated macrophages and eosinophils to infective larvae provides an in vitro surrogate for granuloma formation in vivo . (
  • Here, we describe studies in Cx3cr1 −/− mice and demonstrate the role of Cx3cr1 in the pathoetiology of granuloma formation during acute schistosomiasis. (
  • If, however, a person's symptoms are too troublesome to wait for months, then the granuloma can be surgically removed, but while still leaving part of the stalk or base projecting from the surface, so as to avoid re-injuring the cartilage and perichondrium, which would provoke the formation of another granuloma. (
  • A similar disorder, named granuloma gluteale adultorum, is rarely observed in bed-ridden adults with incontinence ( incontinence-associated dermatitis ). (
  • Mice that are deficient in T lymphocytes (such as TCR α β knockout mice) ( 15 ), B1 B lymphocytes (such as CBA/N mice) ( 9 ), or both (such as SCID mice) ( 8 ) fail to form such granulomas. (
  • These data confirm that BmALT-2 is the antigenic target of granuloma-mediated killing of B. pahangi L3. (
  • If a calcified granuloma is causing symptoms, surgery may be necessary to remove it, according to Mayo Clinic. (
  • Some individuals with contact granulomas have no symptoms whatsoever and only discover they have a granuloma while being examined for some other reason. (
  • Conclusion As the virtual granuloma size increased and the location became more posterior, glottic deposition and ideal particle size generally increased. (
  • In cases of CGD, granulomas may develop due to the body's wounds being unable to properly heal, notes the American Academy of Allergy, Asthma and Immunology. (
  • What is the treatment and outcome for granuloma gluteale infantum? (
  • 1. Lotan G, Klin B, Efrati Y. Double-ligature: a treatment for pedunculated umbilical granulomas in children. (
  • 2 In reality, it is effective for large pedunculated granulomas and avoids a prolonged and usually unsuccessful trial of conservative treatment. (
  • Despite Dr. Wooltorton's observations, we still consider the double-ligature technique to be an attractive option for the treatment of pedunculated umbilical granulomas in children, when the conservative treatments fail. (
  • Granuloma gluteale infantum is a rare form of napkin dermatitis in which there are reddish-purple nodules in the napkin (diaper) area of infants. (
  • Granuloma gluteale infantum is characterised by asymptomatic firm erythematous or violaceous nodules. (