During initial stages of pathogen recognition during tuberculosis infection, neutrophils provide significant immune resistance. This is exhibited by phagocytosis of the pathogen, apoptosis, activation of downstream immune responses, etc. As pathogen recognition by neutrophil cell surface receptor and phagocytosis marks the initial step in any immune response, knowledge on receptor modulations during tuberculosis infection will augment drug designing strategies for the disease. Thus we studied the phagocytosis potential and expression of toll like receptors (TLR1, TLR2 and TLR4) and Fcγ receptors (CD64 and CD32) by human neutrophils following infection with Mycobacterium tuberculosis strains. It is observed that expression of neutrophil TLR2, TLR4 and CD64 is increased in pulmonary tuberculosis patients (PTB) (Median fluorescence intensity (MFI) values of TLR2, TLR4, CD64: 20, 69, 31 respectively) compared to healthy volunteers (HV) (14, 20, 6) registering that MTB recognition and generation of immune response through these receptors becomes quick after acquiring the disease. Nevertheless, the potential of neutrophils to phagocytose E. coli get deteriorated with tuberculosis infection (% HV neutrophils Vs % PTB neutrophils undergoing phagocytosis: 75 Vs 50 & P < 0.001). Meanwhile all the mycobacterial strains studied are more efficient in modulating TLRs compared to Fcγ receptors.
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