Table 1.

Studies suggesting a role for neutrophils in NTM infection

Study models/Reference	Mycobacteria sp	Intervention	Observations
Mouse intravenously infected 106 CFU [38]	M. avium	Neutrophils of C57BL/6 mice infused into susceptible beige mice	Decreased the growth rate of M. avium compared to control beige mice
		Neutrophil depletion in C57BL/6 mice	Increased growth rate compared to control C57BL/6 mice
Mouse 106 CFU or 30 mg LPS intraperitoneally 5 × 104 CFU or 5 mg of LPS intratracheally [39]	M. avium	Gene-disrupted (CXCR2−/−) mice infected with M. avium or treated with LPS intraperitoneally/ intratracheally	Early and rapid recruitment of neutrophils with M. avium infection significantly impaired with CXCR2 chemokine signalling defect compared to controls
Mouse intraperitoneally infected 108 CFU [27]	M. avium	Intravenous inoculation of mycobacteria into CD-l mice	Neutrophil phagocytosis caused degradation of the bacteria and release of enzymatic granules (lactoferrin) that increase macrophage effectiveness in eliminating mycobacteria and enhancing the further killing process
Mouse intravenously infected 107 CFU [40]	M. avium	Administration of G-CSF into C57BL/6 black mice	Neutrophils showed anti-mycobacterial activity. Neutrophil activation inhibited growth compared with control
Mouse intravenously infected 106 CFU [34]	M. avium	TLR2−/− deficient mice infected with M. avium	Defect in early recruitment of neutrophils as compared to the control wild-type (WT)
Mouse intratracheally inoculated 8 × 107 CFU [41]	M. abscessus	Wild type and cystic fibrosis mice inoculated with mycobacteria	Infection causes greater host inflammatory response based on high neutrophil number in the bronchoalveolar lavage of mice infected with rough morphotype compared to smooth morphotype in both type

CFU Colony Forming Unit, G-CSF Granulocyte-Colony Stimulating Factor, LPS lipopolysaccharide