Mucosal immune responses in the trachea after chronic infection withMycoplasma gallisepticumin unvaccinated and vaccinated mature chickens

Abstract

Tracheitis associated with the chronic respiratory disease in chickens caused by Mycoplasma gallisepticum is marked by infiltration of leukocytes into the mucosa.Although cytokines/chemokines are known to play a key role in the recruitment, differentiation, and proliferation of leukocytes, those that are produced and secreted

Immune Evasion of Mycoplasma gallisepticum: An Overview

“…However, the vaccinated birds did not have significantly greater numbers of CD4 + or CD8 + lymphocytes in their tracheal mucosa [ 10 , 107 ]. In unvaccinated chicken, CD8 + cells peaked at 1 week and then declined significantly in the tracheal mucosa [ 3 ] and similar changes in CD8 + cell number and distribution were observed in the tracheal mucosa of infected turkeys [ 107 ]. However, these cells were shown to be CD8 + TCR − cells by double immunohistochemical staining of TCR and CD8 and are likely to be NK or NK-like cells, which are involved in the initial, possibly non-specific, inflammatory response and may be related to the pathogenesis of M. gallisepticum in the trachea [ 11 ], as increased expression of various chemokines and proinflammatory cytokines was observed one week post-M. gallisepticum infection [ 4 ].…”

“…In another study, B cells were detected three weeks after infection with the AP3AS strain of M. gallisepticum in eight-week-old birds and only CD8 + and CD4 + T cells were observed in the first week [ 11 ]. Recently, it was found that B cell recruitment into the mucosa in mature birds occurred later than that in young birds and is generally detectable two weeks after infection [ 3 ]. Birds under four weeks of age likely have a stronger immune response and more severe damage than mature birds, with greater concentrations of M. gallisepticum in the trachea, which may be related to the maturity of the immune system [ 104 ], especially BALT, whose structure, morphology, and ability to perform defense functions in birds are largely age-dependent.…”

“…In contrast, GT5-vaccinated chickens were found to have lower numbers of infiltrating lymphocytes, with more B-cells organized in a typical follicular pattern one week after infection. Chickens vaccinated with ts304 showed a similar situation, with no CD3 + , CD4 + , or CD8 + cells detected in the tracheal mucosa two weeks after challenge at 60 weeks of age [ 3 ]. B cells without help from CD4 + cells are commonly Th-independent and mainly secrete IgM, which promotes M. gallisepticum clearance and reduces the severity of the damage.…”

“…In the one to two weeks after M. gallisepticum infection, there is an acute phase characterized as immune dysregulation. During this period, mycoplasma lipoproteins activate pattern recognition molecules (PRMs), such as TLR2/4/7/15, inducing the expression of cytokines and chemokines, including C-X-C motif chemokine ligand (CXCL)13, CXCL14, C-C motif chemokine ligand 5 (CCL5/RANTES), and interleukin 1β (IL-1β) [ 3 , 4 ]. Large numbers of lymphocytes infiltrate the tracheal tissues, causing local inflammation, but phagocytosis is not fully activated, especially in the absence of specific antibodies [ 5 , 6 , 7 ].…”

“…Mycoplasma may suppress the immune response to some extent, thus allowing the persistence of the infection. It was found that CD8 + T cells were absent in the acute phase [ 3 , 8 ] and that the predominant type of antibody secreted by B cells as well as the amount and pattern of B cell infiltration differed between unvaccinated and vaccinated chickens [ 3 , 9 , 10 ]. The suppression of the adaptive immune response by M. gallisepticum may be crucial to the progression of the disease as local antibodies and cell-mediated immunity are effective in clearing and preventing M. gallisepticum infection [ 11 ].…”