The primary aim of this study was to investigate the alteration of serum inflammatory cytokines during active TB in humans. The changes in cytokine levels were associated with different phenotypes of the disease. The patients were divided into three groups: those with PTB and healthy controls (HC). The sera of TB patients induced a significantly higher pyknosis (swelling) of the nuclei than the sera from HHC and healthy controls. In addition, the serum of TB cases induced an increased number of neutrophils than those of the control group. However, the anti-mycobacterial antibody did not participate in the inflammatory response.
The researchers compared the levels of circulating cytokines in APTP and healthy control groups. The serum of patients with active pulmonary tuberculosis increased IL-1b and decreased TNF-alpha and reduced IL-17A in comparison to healthy controls. They found that the level of IL-1b was associated with disease severity and the time to culture conversion.
The results suggested that a decreased level of IL-2 and IL-6 in the blood of patients with active pulmonary tuberculosis was associated with a lower rate of cure. Moreover, lower levels of IL-17 in patients with active TB were associated with decreased T cell proliferation and enhanced T-cell activation. The researchers concluded that these changes could suggest the immunopathogenic features of tuberculosis.
This study also showed that the circulating levels of proinflammatory cytokines were elevated in APTB patients. These changes may play a role in the immune response to M tuberculosis and may serve as useful indicators for therapeutic success. Further studies may be needed to validate the findings in multiple settings. This is a timely study to follow.
Interestingly, there were significant differences between the levels of IL-2 in TB patients. In addition, IL-6 and IFN-g were reduced in patients with TB. These changes were related to the levels of CD127 and IL-XLR-protease in TB. The researchers further analyzed these findings to identify the role of these cytokines in TB.
This study also found that IL-2 and IL-6 were significantly associated with the disease severity and the time it took to convert cultures. In the same way, IL-10 was associated with the length of time to culture conversion. These results indicate that IL-2 and IL-6 were not necessarily associated with the duration of LTBI. Therefore, this research has important implications for treating pulmonary tuberculosis and predicting its outcome.
The level of IL-1b in pulmonary tuberculosis patients is also associated with the disease severity, with elevated levels of these proteins affecting the time to culture conversion. In addition, the study showed that monocytes were more likely to show a decreased cytotoxicity in the absence of IL-7. These findings indicated that the cellular immune system was not able to effectively combat the disease without IL-17A.
The levels of IL-2 and TNF-g were higher than those of IL-10 and IL-4 in APTB patients. The authors attributed these differences to the failure of the host immune system to control the invading Mtb. They determined the cytokine levels in APTB patients and HC individuals, which were both inflamed.
IL-1b was found to be associated with bacterial burdens in patients with APTB. The depressed gamma interferon levels were linked with bacterial burdens in the patients. The depressed IL-1b levels in APTB were correlated with both bacterial burdens and the time to culture conversion. Similarly, low levels of IL-1b were found in HC.
These cytokines are essential for the immune response against Mtb. The induction of IFNg is regulated by IL-12, which is produced by antigen-presenting cells. Among the patients with advanced TB, plasma levels of IFNg are highest. They decrease after ATT. Similarly, tumor necrosis factor-a is crucial for the control of Mtb infection in animal models.
