CXCL8 and pulmonary tuberculosis: Since IP-10/CXCL10 is involved in trafficking and activation of Th1 lymphocytes [17], and IL-8/CXCL8, in addition to chemotaxis, also reduces the survival of MTb within infected macrophages [13], the up-regulation of NRF in AM and PBMC of active pulmonary TB patients with high bacterial load to repress IP-10/CXCL10 and IL-8/CXCL8 release may render MTb to attenuate host innate immunity attacks resulting in prolonged survival and increased proliferation.