Singh, Nisha and Ahmad, Zeeshan and Baid, Navin and Kumar, Ashwani (2018) Host heme oxygenase-1: Friend or foe in tackling pathogens? IUBMB life, 70 (9). pp. 869-880. ISSN 1521-6551
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Infectious diseases are a major challenge in management of human health worldwide. Recent literature suggests that host immune system could be modulated to ameliorate the pathogenesis of infectious disease. Heme oxygenase (HMOX1) is a key regulator of cellular signaling and it could be modulated using pharmacological reagents. HMOX1 is a cytoprotective enzyme that degrades heme to generate carbon monoxide (CO), biliverdin, and molecular iron. CO and biliverdin (or bilirubin derived from it) can restrict the growth of a few pathogens. Both of these also induce antioxidant pathways and anti-inflammatory pathways. On the other hand, molecular iron can induce proinflammatory pathway besides making the cellular environment oxidative in nature. Since microbial infections often induce oxidative stress in host cells/tissues, role of HMOX1 has been analyzed in the pathogenesis of number of infections. In this review, we have described the role of HMOX1 in pathogenesis of bacterial infections caused by Mycobacterium species, Salmonella and in microbial sepsis. We have also provided a succinct overview of the role of HMOX1 in parasitic infections such as malaria and leishmaniasis. In the end, we have also elaborated the role of HMOX1 in viral infections such as AIDS, hepatitis, dengue, and influenza. © 2018 IUBMB Life, 70(9):869-880, 2018.
| Item Type: | Article |
|---|---|
| Additional Information: | Copyright of this article belongs to Wiley. |
| Uncontrolled Keywords: | Candida; HIV; Leishmania; Mycobacterium; Plasmodium; Salmonella; carbon monoxide; dengue; heme oxygenase 1; hepatitis; influenza and microbial infections; malaria; sepsis; tuberculosis |
| Subjects: | Q Science > QR Microbiology |
| Depositing User: | Dr. K.P.S.Sengar |
| Date Deposited: | 18 Mar 2019 16:46 |
| Last Modified: | 18 Mar 2019 16:46 |
| URI: | http://crdd.osdd.net/open/id/eprint/2163 |
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