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Review
. 2022 Jul 22:12:870398.
doi: 10.3389/fcimb.2022.870398. eCollection 2022.

Redox Imbalance and Its Metabolic Consequences in Tick-Borne Diseases

Monika Groth  1 , Elżbieta Skrzydlewska  2 , Marta Dobrzyńska  2 , Sławomir Pancewicz  1 , Anna Moniuszko-Malinowska  1
Affiliations
Review

Redox Imbalance and Its Metabolic Consequences in Tick-Borne Diseases

Monika Groth et al. Front Cell Infect Microbiol. .

Abstract

One of the growing global health problems are vector-borne diseases, including tick-borne diseases. The most common tick-borne diseases include Lyme disease, tick-borne encephalitis, human granulocytic anaplasmosis, and babesiosis. Taking into account the metabolic effects in the patient's body, tick-borne diseases are a significant problem from an epidemiological and clinical point of view. Inflammation and oxidative stress are key elements in the pathogenesis of infectious diseases, including tick-borne diseases. In consequence, this leads to oxidative modifications of the structure and function of phospholipids and proteins and results in qualitative and quantitative changes at the level of lipid mediators arising in both reactive oxygen species (ROS) and ROS enzyme-dependent reactions. These types of metabolic modifications affect the functioning of the cells and the host organism. Therefore, links between the severity of the disease state and redox imbalance and the level of phospholipid metabolites are being searched, hoping to find unambiguous diagnostic biomarkers. Assessment of molecular effects of oxidative stress may also enable the monitoring of the disease process and treatment efficacy.

Keywords: Lyme; oxidative stress; redox; tick-borne; tick-borne encephalitis.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Effect of pathogens on interaction between ROS generation and inflammation in host organism.
Figure 2
Figure 2
Effect of pathogens on phospholipid metabolism in host organism.
Figure 3
Figure 3
Redox imbalance and metabolic effects of B. burgdorferi.
Figure 4
Figure 4
Changes in phospholipid metabolism with lipid mediators generation during B. burgdorferi infection.
Figure 5
Figure 5
Effects of pathogen–vector–host interactions in TBE infection.
See this image and copyright information in PMC

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