Table 3. Potential effects of SHS/direct CS on neutrophil function against TB.

Neutrophil phenotype and function	Effects of SHS/direct CS
Migration of neutrophils	Smokers have three- to four-fold more neutrophils in the lungs than non-smokers, likely due to CS induction of IL-8 and IL-17, the latter through CS differentiation of TH17 cells (71,77)(H,M).
Neutrophil activation	PD-L1 is increased on neutrophils of active TB patients (78)(H) and CS, nicotine, and lipopolysaccharide (a common contaminant of cigarettes) are known to induce PD-L1/2 expression (57,58)(M,H), theoretically deactivating neutrophils, leading to formation of non-protective, necrotic granulomas (75)(M/H).
Oxidative burst	CS inhibited endogenous oxidative burst (79)(H).
Induction of (N2) neutrophils	Lipopolysaccharide found in cigarettes induced the expression of immunosuppressive N2 (CD16hiCD62LloCD11bhiCD54hi) neutrophils, which inhibit T cell proliferation (76)(H).
NETs	CS inhibited endogenous oxidative burst — which is required for NETs formation; thus, CS could inhibit formation of NETs (79,80)(H,M/H)

M, murine; H, human; M/H, murine and human; NET, neutrophil extracellular trap.