The Interplay between Innate Immunity and Cardiovascular Diseases in Animals

Nebojsa Munir^*
*Correspondence: Nebojsa Munir, Department of Anesthesiology, Advocate Illinois Masonic Medical Center, 836 W. Wellington Ave. Suite 4815, Chicago, IL 60657, USA, Email:

Introduction

Cardiovascular Diseases (CVDs) are a leading cause of mortality and morbidity in animals, just as they are in humans. While the pathogenesis of CVDs in animals shares similarities with humans, there are distinct differences, including the role of innate immunity. Understanding how the innate immune system contributes to CVDs in animals is crucial for developing effective preventive and therapeutic strategies. This article explores the intricate interplay between innate immunity and cardiovascular diseases in animals [1]. The innate immune system serves as the first line of defense against pathogens and tissue injury in animals. Components of innate immunity include physical barriers, such as the skin and mucous membranes, as well as cellular and molecular mechanisms like phagocytes, natural killer cells and cytokines. Innate immunity plays a pivotal role in maintaining tissue homeostasis and responding to insults that contribute to cardiovascular diseases. Atherosclerosis, a hallmark of CVDs, is characterized by the accumulation of lipid-laden plaques in arterial walls. Innate immune cells, particularly macrophages and dendritic cells, contribute to the initiation and progression of atherosclerosis through inflammatory processes. Lipid accumulation triggers an inflammatory response, leading to the recruitment of immune cells and the production of pro-inflammatory cytokines, perpetuating plaque formation and instability. PRRs, such as Toll-Like Receptors (TLRs) and scavenger receptors, recognize Pathogen-associated Molecular Patterns (PAMPs) and DamageAssociated Molecular Patterns (DAMPs) released during tissue injury. Activation of PRRs in arterial cells and immune cells triggers inflammatory signaling cascades, exacerbating atherosclerosis and promoting plaque rupture. Genetic variations in PRRs influence susceptibility to CVDs in animals, highlighting the importance of innate immune pathways in disease pathogenesis [2].

Description

The complement system, a crucial component of innate immunity, contributes to CVD pathogenesis through various mechanisms. Dysregulation of complement activation promotes endothelial dysfunction, smooth muscle cell proliferation and plaque progression. Therapeutic targeting of complement components shows promise in mitigating CVD progression in animal models, underscoring the therapeutic potential of modulating innate immune pathways. Genetic predisposition influences susceptibility to CVDs in animals, with certain breeds exhibiting increased risk due to inherited traitsaffecting immune function and lipid metabolism. Environmental factors, such as diet, stress and exposure to pollutants, modulate innate immune responses and contribute to CVD development in animals.Targeting innate immune pathways holds promise for the prevention and treatment of CVDs in animals. Immunomodulatory agents, including anti-inflammatory drugs and monoclonal antibodies targeting specific immune mediators, show potential in reducing plaque inflammation and stabilizing atherosclerotic lesions. Nutritional interventions and lifestyle modifications that modulate innate immune function may complement conventional therapies for managing CVDs in animals.

Conclusion

Understanding the intricate interplay between innate immunity and cardiovascular diseases in animals provides insights into disease pathogenesis and therapeutic targets. Harnessing the immunomodulatory potential of innate immune pathways offers promising avenues for the prevention and treatment of CVDs in veterinary medicine. Further research is warranted to elucidate the specific mechanisms underlying innate immune dysregulation in different animal species and translate these findings into clinical practice for improved cardiovascular health in animals.

References

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