In vitro granuloma formation, no production and cytokines profile from human mononuclear cells induced by fractionated antigens of paracoccidioides brasiliensis

Paracoccidioidomycosis

“…In either case, neutrophils are present in tissues and participate in granuloma formation largely contributing to the inflammatory response [52]. The major biological significance of granuloma is the limitation of the infection to a local area but if such formation is loose, dissemination would ensue [1,53].…”

Interleukin-10 and Tumor Necrosis Factor–α Single Nucleotide Gene Polymorphism Frequency in Paracoccidioidomycosis

“…Therefore, imbalance in the Th1/Th2 paradigm reflects a decreased ability to control this infection. The granulomatous inflammation is typical of PCM and is a putative mechanism to overcome the infection [3][4][5]. In general, cytokines are involved in many diseases and, consequently, many studies have been conducted to investigate whether a genetic basis for these diseases may be found in polymorphisms of cytokine genes [6 -8].…”

“…Although IL-10 limits inflammatory responses, tumor necrosis factor-␣ (TNF-␣) determines the strength and the length of local and systemic inflammatory reactions [11]. This cytokine is involved in the resistance to Pb infection, granuloma formation, and control of fungus dissemination [4,15]. In addition, TNF-␣ modulates the production of other cytokines and nitric oxide, as well as the T-cell proliferative response in Pb-infected mice [15,16].…”

Intercellular Adhesion Molecule-1 Is Required for the Early Formation of Granulomas and Participates in the Resistance of Mice to the Infection with the Fungus Paracoccidioides brasiliensis

“…8 The stimulation of a variety of cells, such as endothelial, mesangial, and bronchial epithelial cells, with inflammatory cytokines [interleukin (IL)-1, TNF-␣, and IFN-␥] increases expression of ICAM-1 12 and favors the transendothelial migration of leukocytes through the interaction with ␤2 integrins. 11,12 The levels of inflammatory cytokines TNF-␣, IL-1, IL-6, IL-12, and IFN-␥ 6,7,[13][14][15][16][17][18][19][20] are increased during the infection with P. brasiliensis. Expression of ICAM-1 is also greatly increased in the lungs of mice infected with conidial forms of P. brasiliensis 21 and is a probably a consequence of the production of proinflammatory cytokines.…”