Apoptosis and Autophagy: Current Understanding in Tick–Pathogen Interactions

Abstract

Tick-borne diseases are a significant threat to human and animal health throughout the world. How tick-borne pathogens successfully infect and disseminate in both their vertebrate and invertebrate hosts is only partially understood. Pathogens have evolved several mechanisms to combat host defense systems, and to avoid and modulate host immunity during infection, therefore benefitting their survival and replication. In the host, pathogens trigger responses from innate and adaptive immune systems that recognize and eliminate invaders. Two important innate defenses against pathogens are the programmed cell death pathways of apoptosis and autophagy. This Mini Review surveys the current knowledge of apoptosis and autophagy pathways in tick-pathogen interactions, as well as the strategies evolved by pathogens for their benefit. We then assess the limitations to studying both pathways and discuss their participation in the network of the tick immune system, before highlighting future perspectives in this field. The knowledge gained would significantly enhance our understanding of the defense responses in vector ticks that regulate pathogen infection and burden, and form the foundation for future research to identify novel approaches to the control of tick-borne diseases.

Could lipocalin 2 be involved in the effects of iron overload and a high-fat diet on neuronal death? An exploratory study

“…This nding is in line with the decrease of BIM expression seen in adipocytes of obese people and mice submitted to a HFD protocol. According to Wang and Cull (2022), this decrease in BIM expression could be caused by the activation of the transcriptional cofactors YAP (Yes-associated protein) and TAZ (transcriptional coactivator with PDZ-binding motif) and the increase in the translocation of the YAP/TAZ complex to the nucleus, where it would downregulate the expression of the BIM gene and protect the adipocytes against apoptosis (Wang and Cull 2022). Although there are no studies about the association of HFD and increased activity on the YAP/TAZ complex in the nervous system, Hoshino and colleagues (2006) found a neuron speci c isoform of YAP, the YAPdeltaC, that protects against apoptosis and shows increased levels in animal models of Huntington Disease, suggesting a pro-survival effect for YAPdeltaC (Hoshino et al 2006).…”

Exotoxins from <em>Clostridium septicum</em> Kill Mouse Peritoneal Macrophages: A Possible Mechanism of Bacterial Immune-Evasion at Infection Sites

“…Moreover, the exposure of macrophages to 1% PPF≥100kDa induced autophagy over time (until 4 h). Autophagy is an important process that induces apoptotic cell death in response to microbial toxins [1]. In addition, autophagy induced by PPF could be classified as cell death associated with autophagy, giving an advantage to C. septicum during infection.…”

“…A surprising feature of myonecrotic disease caused by clostridia is the absence of phagocytic cells at the infection site [1]. Circulating monocytes are recruited at the injury site where they differentiate into tissue macrophages.…”

Serpins in Tick Physiology and Tick-Host Interaction

“…To prevent rejection by the host, ticks use a mixture of pharmacologically active molecules at the site of injury to manipulate all types of host immune responses. Many excellent and thorough review articles have been published describing both the immune response against tick attachment and the effects of tick saliva or of individual salivary compounds on the host immune system ( Hovius et al., 2008 ; Francischetti et al., 2009 ; Kazimírová and Štibrániová, 2013 ; Kotál et al., 2015 ; Chmelař et al., 2016 ; Chmelař et al., 2017 ; Kazimírová et al., 2017 ; Šimo et al., 2017 ; Chmelař et al., 2019 ; Wen et al., 2019 ; Aounallah et al., 2020 ; Martins et al., 2020 ; Fogaça et al., 2021 ; Jmel et al., 2021 ; Narasimhan et al., 2021 ; Wikel, 2021 ; Wang and Cull, 2022 ). In the following section, we discuss how tick salivary serpins contribute to the evasion of immunity-mediated host defense mechanisms – both innate ( Figure 4 ) and adaptive ( Figure 5 ).…”