Abdel-Rahman Youssef
Turkish Journal of Immunology - 2025;13(3):169-176
Objective: Haemophilus influenzae is a Gram-negative bacterium that commonly colonizes and infects the respiratory tract. The bacterial infection may modulate host immune responses. However, the T cell responses to H. influenzae remain unclear.. This study aimed to investigate the CD4+ T cell responses to live strains of typeable H. influenzae (THi) and non-typeable H. influenzae (NTHi) in vitro. Materials and Methods: CD4+ T cells were isolated from healthy individuals and infected with live variants of a single strain of THi (132b+, 132b-, 132b-p5-) and NTHi (A950002, A950002p5-, A850052, d1, d3). The CD4 + T cell responses to H. influenzae were investigated in vitro by evaluating the cell proliferation using a [³H]-thymidine incorporation assay and measuring the levels of T helper-1 (Th1) cytokines (interferon-gamma [IFN-gamma], tumor necrosis factor-alpha [TNF-alpha]) and Th2 cytokines (interleukin-5 [IL-5], interleukin-10 [IL-10]) using a human Th1/Th2 cytokine cytometric bead array (CBA). Results: Both NTHi strains and THi are bound to CD4 + T cells to variable degrees, and the presence of the P5 protein in H. influenzae P5+ strains increased the binding to CD4 + T cells significantly compared to P5-deficient strains (132b- vs. 132b-p5- [p= 0.0009], A950002 vs. A950002p5 [p=0.0039], d1 vs. d3 [p=0.0014]). THi (132b-, 132b-p5) and NTHi strains (A850052, d1, d3) caused marked inhibition of CD4 + T cell proliferation (p< 0.0001). NTHi strains (A850052, d1, d3) significantly suppressed IFN-gamma, TNF-alpha, IL-5, and IL-10 production (p<0.0001). THi strains 132b- and 132b-p5- markedly suppressed IFN-gamma production (p<0.0001). TNF-alpha production was significantly inhibited by132b- strain (p=0.0002), and A950002 strain (p=0.01). IL-5 production was reduced by all THi and NTHi strains (p<0.0001), while all THi and some NTHi strains (A850052, d1, d3) decreased IL-10 production (p<0.0001). Conclusion: These results suggest that the immunosuppressive effects of certain strains of H. influenzae may represent a mechanism by which the bacterium evades the adaptive immune response, facilitating the establishment of respiratory colonization and persistence of the infection.
