scholarly journals A Role for CD154, the CD40 Ligand, in Granulomatous Inflammation

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Julien Villeneuve ◽  
Alexis Desmoulière ◽  
Antoine Dewitte ◽  
Nelly Bordeau ◽  
Pierre Costet ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Granulomatous Inflammation ◽  
Cd40 Ligand ◽  
Giant Cells ◽  
Absorbable Suture ◽  
Epithelioid Cells ◽  
History Of ◽  
Toxic Liver Injury ◽  
Deficient Mice

Granulomatous inflammation is a distinctive form of chronic inflammation in which predominant cells include macrophages, epithelioid cells, and multinucleated giant cells. Mechanisms regulating granulomatous inflammation remain ill-understood. CD154, the ligand of CD40, is a key mediator of inflammation. CD154 confers a proinflammatory phenotype to macrophages and controls several macrophagic functions. Here, we studied the contribution of CD154 in a mouse model of toxic liver injury with carbon tetrachloride and a model of absorbable suture graft. In both models, granulomas are triggered in response to endogenous persistent liver calcified necrotic lesions or by grafted sutures. CD154-deficient mice showed delayed clearance of carbon tetrachloride-induced liver calcified necrotic lesions and impaired progression of suture-induced granuloma. In vitro, CD154 stimulated phagocytosis of opsonized erythrocytes by macrophages, suggesting a potential mechanism for the altered granulomatous inflammation in CD154KO mice. These results suggest that CD154 may contribute to the natural history of granulomatous inflammation.

Equine Granulomatous Enteritis

1974 ◽  
Vol 11 (6) ◽  
pp. 535-547 ◽  
Author(s):  
R. E. Cimprich
Keyword(s):  
Weight Loss ◽  
Mycobacterium Tuberculosis ◽  
Plasma Cells ◽  
Granulomatous Inflammation ◽  
Giant Cells ◽  
Gut Content ◽  
Epithelioid Cells ◽  
History Of ◽  
Microscopic Change ◽  
Granulomatous Enteritis

The gross abnormalities in the intestines of 10 horses with a history of chronic weight loss varied greatly. The principal microscopic change was granulomatous inflammation characterized by lymphocytes, plasma cells, macrophages, epithelioid cells and giant cells. Mycobacterium tuberculosis, avian type, was isolated from the gut content of one horse, but no cause was found in the others. Horses previously reported to have tuberculosis had lesions similar to those described here. These lesions are also similar to those in Crohn's disease of man.

scholarly journals Blastomycosis Presenting as Multiple Splenic Abscesses: Case Report and Review of the Literature

2010 ◽  
Vol 21 (1) ◽  
pp. 53-56 ◽  
Author(s):  
Sami Al-Nassar ◽  
Tracy MacNair ◽  
Jeremy Lipschitz ◽  
Howard Greenberg ◽  
Elly Trepman ◽  
...  
Keyword(s):  
Granulomatous Inflammation ◽  
Giant Cells ◽  
Silver Stain ◽  
Rare Presentation ◽  
Computed Tomographic ◽  
Northwestern Ontario ◽  
Abdominal Symptoms ◽  
History Of ◽  
Oral Itraconazole ◽  
Methenamine Silver Stain

A 31-year-old Canadian Aboriginal man from northwestern Ontario presented with left upper quadrant pain and a tender left upper quadrant mass. Evaluation with a computed tomography scan showed multiple lesions within the spleen, a collection between the splenic tip and splenic flexure of the colon, and several small adrenal lesions. Computed tomographic-guided needle biopsy showed necrotizing granulomatous inflammation and multinucleated giant cells. Gomori’s methenamine silver stain showed broad-based budding yeast consistent withBlastomyces dermatitidis. Abdominal symptoms resolved after two months of oral itraconazole. Multiple splenic abscesses are a rare presentation of blastomycosis and should be considered in the differential diagnosis of left upper quadrant abdominal pain in a patient with a history of travel or residence in a region endemic forB dermatitidis.

scholarly journals NLRC5 Deficiency Deregulates Hepatic Inflammatory Response but Does Not Aggravate Carbon Tetrachloride-Induced Liver Fibrosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Akouavi Julite I. Quenum ◽  
Akhil Shukla ◽  
Fjolla Rexhepi ◽  
Maryse Cloutier ◽  
Amit Ghosh ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Fibrosis ◽  
Inflammatory Response ◽  
Receptor Gene ◽  
Cell Types ◽  
Matrix Metalloproteinase 3 ◽  
Collagen Genes ◽  
And Control ◽  
Deficient Mice

The nucleotide-binding leucine-rich repeat-containing receptor (NLR) family protein-5 (NLRC5) controls NF-κB activation and production of inflammatory cytokines in certain cell types. NLRC5 is considered a potential regulator of hepatic fibrogenic response due to its ability to inhibit hepatic stellate activation in vitro. To test whether NLRC5 is critical to control liver fibrosis, we treated wildtype and NLRC5-deficient mice with carbon tetrachloride (CCl4) and assessed pathological changes in the liver. Serum alanine transaminase levels and histopathology examination of liver sections revealed that NLRC5 deficiency did not exacerbate CCl4-induced liver damage or inflammatory cell infiltration. Sirius red staining of collagen fibers and hydroxyproline content showed comparable levels of liver fibrosis in CCl4-treated NLRC5-deficient and control mice. Myofibroblast differentiation and induction of collagen genes were similarly increased in both groups. Strikingly, the fibrotic livers of NLRC5-deficient mice showed reduced expression of matrix metalloproteinase-3 (Mmp3) and tissue inhibitor of MMPs-1 (Timp1) but not Mmp2 or Timp2. Fibrotic livers of NLRC5-deficient mice had increased expression of TNF but similar induction of TGFβ compared to wildtype mice. CCl4-treated control and NLRC5-deficient mice displayed similar upregulation of Cx3cr1, a monocyte chemoattractant receptor gene, and the Cd68 macrophage marker. However, the fibrotic livers of NLRC5-deficient mice showed increased expression of F4/80 (Adgre1), a marker of tissue-resident macrophages. NLRC5-deficient livers showed increased phosphorylation of the NF-κB subunit p65 that remained elevated following fibrosis induction. Taken together, NLRC5 deficiency deregulates hepatic inflammatory response following chemical injury but does not significantly aggravate the fibrogenic response, showing that NLRC5 is not a critical regulator of liver fibrosis pathogenesis.

In Vitro Formation of Macrophage- Epithelioid Cells and Multinucleated Giant Cells by 1?,25-Dihydroxyvitamin D3from Human Circulating Monocytes

1986 ◽  
Vol 465 (1 Tenth Interna) ◽  
pp. 211-220 ◽  
Author(s):  
MASATAKA OHTA ◽  
TETSURO OKABE ◽  
KEIYA OZAWA ◽  
AKIO URABE ◽  
FUMIMARO TAKAKU
Keyword(s):  
Giant Cells ◽  
Multinucleated Giant Cells ◽  
Epithelioid Cells

scholarly journals P2X7Receptor and Polykarion Formation

2000 ◽  
Vol 11 (9) ◽  
pp. 3169-3176 ◽  
Author(s):  
Simonetta Falzoni ◽  
Paola Chiozzi ◽  
Davide Ferrari ◽  
Gary Buell ◽  
Francesco Di Virgilio
Keyword(s):  
Cell Fusion ◽  
Cell Formation ◽  
Granulomatous Inflammation ◽  
Giant Cells ◽  
Mononuclear Phagocytes ◽  
Cell Contact ◽  
Giant Cell Formation ◽  
High Level ◽  
Multinucleated Giant Cell Formation

Cell fusion is a central phenomenon during the immune response that leads to formation of large elements called multinucleated giant cells (MGCs) of common occurrence at sites of granulomatous inflammation. We have previously reported on the involvement in this event of a novel receptor expressed to high level by mononuclear phagocytes, the purinergic P2X7receptor. Herein, we show that blockade of this receptor by a specific monoclonal antibody prevents fusion in vitro. In contrast, cell fusion is stimulated by addition of enzymes that destroy extracellular ATP (i.e., apyrase or hexokinase). Experiments performed with phagocytes selected for high (P2X7hyper) or low (P2X7hypo) P2X7expression show that fusion only occurs between P2X7hyper/P2X7hyper and not between P2X7hyper/P2X7hypo or P2X7hypo/P2X7hypo. During MGCs formation we detected activation of caspase 3, an enzyme that is powerfully stimulated by P2X7. Finally, we observed that during MGCs formation, the P2X7receptor is preferentially localized at sites of cell-to-cell contact. These findings support the hypothesis originally put forward by our group that the P2X7receptor participates in multinucleated giant cell formation.

scholarly journals A rare association of tonsillar tuberculosis and lichen scrofulosorum

2021 ◽  
Vol 37 (1) ◽  
Author(s):  
Anshika Harit ◽  
Anjan Kumar Sahoo ◽  
Ishwar Singh
Keyword(s):  
Sore Throat ◽  
Extrapulmonary Tuberculosis ◽  
Granulomatous Inflammation ◽  
Giant Cells ◽  
Skin Lesions ◽  
Epithelioid Cell ◽  
Body Sensation ◽  
Biopsy Report ◽  
History Of ◽  
Systemic Examination

Abstract Background Both tonsillar tuberculosis and lichen scrofulosorum are sporadic presentations of extrapulmonary tuberculosis. Lichen scrofulosorum commonly presents in children and young adults as lichenoid eruptions over the skin. Granulomatous inflammation of the tonsils, however, presents as non-specific sore throat and foreign body sensation in the throat. The concomitant presentation of the abovementioned tubercular manifestations has not been reported in the literature. Case presentation Herein, we report a case of an 11-year-old male patient who presented with a history of recurrent sore throat and ulcerative lesion over the tonsil. Systemic examination revealed multiple perifollicular eruptions over the trunk and back. The diagnosis was confirmed on histopathological findings of epithelioid cell granulomas with Langerhans giant cells following biopsy from the tonsil and skin lesions. Antitubercular therapy was initiated soon after. The patient responded to treatment as early as 6 weeks and was completely asymptomatic at 1 year of follow-up. Conclusion A diagnosis of granulomatous tonsillitis should alert the physician to the possibility of underlying systemic tuberculosis. In our case, coexistence of lichen scrofulosorum helped us to substantiate the diagnosis based on the biopsy report. Response to antitubercular agents is excellent and should be started at the earliest.

scholarly journals Augmentation of Antigen Receptor–mediated Responses by Histamine H1 Receptor Signaling

1999 ◽  
Vol 189 (4) ◽  
pp. 673-682 ◽  
Author(s):  
Yasmin Banu ◽  
Takeshi Watanabe
Keyword(s):  
B Cells ◽  
Immune Responses ◽  
Antigen Receptor ◽  
Cd40 Ligand ◽  
G Protein Coupled Receptors ◽  
Cross Linking ◽  
T And B Cells ◽  
G Protein Coupled ◽  
Deficient Mice

Histamine is considered one of the important mediators of immediate hypersensitivity and inflammation, and acts via G protein–coupled receptors. Here, we report that histamine may affect antigen receptor–mediated immune responses of T and B cells via a signal(s) from histamine H1 receptors (H1Rs). Histamine exhibited enhancing effects on the in vitro proliferative responses of anti-CD3ε– or anti-IgM–stimulated spleen T and B cells, respectively, at the culture condition that the fetal calf serum was dialyzed before culture and c-kit–positive cells were depleted from the spleen cells. In studies of histamine H1R knockout mice, H1R-deficient T cells had low proliferative responses to anti-CD3ε cross-linking or antigen stimulation in vitro. B cells from H1R-deficient mice were also affected, demonstrating low proliferative responses to B cell receptor cross-linking. Antibody production against trinitrophenyl-Ficoll was reduced in H1R-deficient mice. Other aspects of T and B cell function were normal in the H1R knockout mice. H1R-deficient T and B cells showed normal responses upon stimulation with interleukin (IL)-2, IL-4, CD40 ligand, CD40 ligand plus IL-4, and lipopolysaccharide. Collectively, these results imply that the signal generated by histamine through H1R augments antigen receptor–mediated immune responses, suggesting cross-talk between G protein–coupled receptors and antigen receptor–mediated signaling.

scholarly journals An Uncommon Cause of a Small-Bowel Obstruction

2017 ◽  
Vol 2017 ◽  
pp. 1-4
Author(s):  
Ali Zakaria ◽  
Bayan Al Share ◽  
Issam Turk ◽  
Samira Ahsan ◽  
Waseem Farra
Keyword(s):  
Small Bowel ◽  
Small Bowel Obstruction ◽  
Bowel Obstruction ◽  
Previous History ◽  
Granulomatous Inflammation ◽  
Giant Cells ◽  
Unknown Etiology ◽  
Granulomatous Disease ◽  
History Of ◽  
Noncaseating Granulomas

Sarcoidosis is a systemic granulomatous disease of unknown etiology, characterized by the formation of noncaseating granulomas. Gastrointestinal (GI) system involvement that is clinically recognizable occurs in less than 0.9% of patients with sarcoidosis, with data revealing small intestine involvement in 0.03% of the cases. A high index of suspension is required in patients presenting with small-bowel obstruction and previous history of sarcoidosis. Establishing a definitive diagnosis of GI sarcoidosis depends on biopsy evidence of noncaseating granulomas, exclusion of other causes of granulomatous disease, and evidence of sarcoidosis in at least one other organ system. Treatment of GI sarcoidosis depends on symptomatology and disease activity. Herein, we are presenting a case of 67-year-old female patient who had acute small-bowel obstruction at the level of jejunum with postoperative histopathologic evidence of noncaseating granulomatous inflammation with multinucleated giant cells, consistent with sarcoidosis.

scholarly journals TRANSFORMATION OF MONOCYTES IN TISSUE CULTURE INTO MACROPHAGES, EPITHELIOID CELLS, AND MULTINUCLEATED GIANT CELLS

1966 ◽  
Vol 28 (2) ◽  
pp. 303-332 ◽  
Author(s):  
Jerry S. Sutton ◽  
Leon Weiss
Keyword(s):  
Golgi Apparatus ◽  
Plasma Membranes ◽  
Giant Cells ◽  
Progressive Increase ◽  
Multinucleated Giant Cells ◽  
Epithelioid Cells ◽  
Cytoplasmic Filaments ◽  
Monocytes And Macrophages ◽  
Sequential Transformation

The sequential transformation of chicken monocytes into macrophages, epithelioid cells, and multinucleated giant cells in vitro was studied by electron microscopy after fixation and embedment in situ. The following changes occur. In the nucleus, margination of chromatin, evident in monocytes, decreases in later forms. Nucleoli become more complex and nuclear pores increase in number. In cytoplasm, a progressive increase in volume of the ectoplasm and endoplasm occurs in culture. Lysosomes increase in number and size prior to phagocytosis. During phagocytosis (most active from 1 to 3 days of culture) lysosome depletion occurs. Lysosomes are present in greatest number and show maximal structural variation in the epithelioid and young giant cells. Aging giant cells lose lysosomes. All stages possess variably large quantities of rough-surfaced endoplasmic reticulum and free ribosomes. The Golgi apparatus, small in monocytes, increases in size and complexity. Massive accumulations of lysosomes within the Golgi apparatus of macrophages and epithelioid cells suggest that lysosomes originate there. In giant cells, multiple Golgi regions occur, often ringing the nuclei. Monocytes and macrophages have few mitochondria. Mitochondria of epithelioid cells are larger, more numerous, and may have discontinuous outer membranes. Mitochondria are most numerous in giant cells where they increase with age and become polymorphous. Cytoplasmic filaments are approximately 50 to 60 A in diameter and of indeterminate length. They occur both singly and in bundles which touch cytoplasmic vesicles and mitochondria. Few filaments occur in monocytes and macrophages. A large increase in the number of filaments occurs in epithelioid cells, where filaments (90 to 100 A) surround the cytocentrum as a distinctive annular bundle often branching into the cytoplasm. The greatest concentration of filaments occurs in aged giant cells. Pseudopodia are always present. They are short and filiform in monocytes and giant cells, and broad, with abundant micropinocytotic vesicles, in macrophages and epithelioid cells. At every stage, the cell membrane contains dense cuplike structures. These may represent the membranous residue of lysosomes which have discharged to the outside, analogous to merocrine secretion. Contiguous epithelioid cells display elaborate cytoplasmic interdigitation. In places, the plasma membranes break down and epithelioid cells fuse to form giant cells.

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