Table 1 Studies suggesting a role for neutrophils in NTM infection

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