Interferon-γ inducible protein 10 (IP-10), is a potent chemoattractant that promotes migration of monocytes and activated T-cells to inflammation foci. IP-10 is elevated in serum of patients with chronic hepatitis C virus (HCV) and tuberculosis (TB) infections, although it remains to be determined the contribution of IP-10 in restricting Mycobacterium tuberculosis (Mtb) replication. Here, we investigated the impact of IP-10 on mycobacteria replication using the ex vivo model of human whole-blood (WB) assay. In particular, we compared the levels of IP-10 upon infection with different Mtb clinical strains and species of non-tuberculous mycobacteria (NTM) and evaluated how IP-10 may contain bacterial replication. Interestingly, we observed that the inhibition of the host enzyme dipeptidyl peptidase IV (DPP-IV), which inactivates IP-10 through cleavage of two amino acids at the chemokine N-terminus, restricted mycobacterial persistence in WB, supporting the critical role of full length IP-10 in mediating an anti-Mtb response. Addition of recombinant IP-10 expressed in eukaryotic cells enhanced the anti-mycobacterial activity in WB, although no differences were observed when IP-10 containing different proportions of cleaved and non-cleaved forms of the chemokine were added. Moreover, recombinant IP-10 did not exert a direct anti-mycobacterial effect. Our results underscore the clinical relevance of IP-10 in mycobacteria pathogenesis and support the potential outcomes that may derive by targeting the IP-10/CXCR3 pathway as host directed therapies for the treatment of Mtb or NTM infections.
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http://dx.doi.org/10.1016/j.ijmm.2019.05.005 | DOI Listing |
Alzheimers Dement
December 2024
Department of Neurology, Columbia University, New York, NY, USA.
Background: Alzheimer's disease (AD) is the most common form of dementia. The neurotropic virus herpes simplex virus 1 (HSV1) has been linked to the pathogenesis of AD. While ∼65% of the US population is infected with HSV1, in the majority of cases the virus is dormant and infected individuals are asymptomatic.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Cardiovascular Surgery, Nihon University Hospital, Itabashi-ku, Tokyo, Japan.
We investigated the influence of false lumen (FL) status on the systemic inflammatory response triggered by acute aortic dissection (AAD) using cytokine profiling. The study included 44 patients with AAD. Patients were divided between those with a thrombosed FL (Group T, n = 21) and those with a non-thrombosed FL (Group P, n = 23).
View Article and Find Full Text PDFTuberculosis (Edinb)
December 2024
Clinical Infection Medicine, Department of Translational Medicine, Lund University, Ruth Lundskogs gata 3, SE214 28, Malmö, Sweden.
Background: Interferon-γ release assays (IGRAs) for tuberculosis infection (TBI) cannot distinguish different stages of the TBI spectrum (including spontaneously cleared infection). We investigated patterns of Mtb-specific blood mediators in people with and without TBI during tuberculosis preventive therapy (TPT).
Methods: Individuals with likelihood of recent Mtb exposure, aged 15-25 years, with valid IGRA results, in whom tuberculosis (TB) had been excluded, were included.
Sci Rep
December 2024
Medical Technology Program, Faculty of Science, Nakhon Phanom University, Nakhon Phanom, Thailand.
Interferon γ-induced protein 10 kDa (IP-10) or C-X-C motif chemokine 10 (CXCL10) is produced and secreted from specific leukocytes such as neutrophils, eosinophils, and monocytes, which play key roles in the immune response to Plasmodium infections. This systematic review aimed to collate and critically appraise the current evidence on IP-10 levels in malaria patients. It provided insights into its role in malaria pathogenesis and potential as a biomarker for Plasmodium infections and disease severity.
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