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In many newborn infants, neutropaenia is a self-resolving condition. Nevertheless, it is thought that in premature infants, neutrophil formation and function are a little different. Since neutrophils play a crucial role in innate immunity, neonatal neutropenia in premature infants needs to be quickly identified and treated according to the risk factors, especially those of clinical infections. Numerous factors, including maternal and prenatal conditions, congenital syndromes, immune-mediated processes, nosocomial infections, and idiopathic conditions, can contribute to neutropenia in premature infants. However, not all premature infant neutropaenia is clinically significant and frequently does not increase the risk of infection. In this review article, we\\\'ll talk about the birth of neutrophils, neonatal neutropenia causes, how premature infants and neutropenia are related, and some effective ways to treat the condition.

Trichomonas vaginalis, a prevalent sexually transmitted parasite, poses substantial risks to maternal health during pregnancy, eliciting a multifaceted immune response crucial for host defense. Neutrophils, as primary innate immune effectors, play a pivotal role in combatting this infection within the intricate immunological landscape of pregnancy. This comprehensive review aims to elucidate the complex interplay between Trichomonas vaginalis infection and the dynamic responses of neutrophils in pregnant women, exploring mechanisms of neutrophil recruitment, activation, effector functions, and the parasite\'s evasion strategies. Insights into neutrophil dynamics and activation mechanisms reveal their essential functions in combating T. vaginalis, encompassing chemotaxis, phagocytosis, release of reactive oxygen species, and formation of neutrophil extracellular traps. Furthermore, the review discusses how pregnancy-associated immunomodulation influences neutrophil function in response to this parasitic infection. Concurrently, the elucidation of T. vaginalis evasion tactics—surface antigen variation, adhesion strategies, and immune subversion—underscores the complexity of host-parasite interactions and the challenges faced by neutrophils in eradicating the parasite. Considering the clinical implications, particularly adverse pregnancy outcomes and maternal morbidity associated with T. vaginalis infection, the review addresses current treatment modalities, management challenges during pregnancy, and potential therapeutic strategies targeting neutrophil responses and immune modulation. In conclusion, understanding the intricate interplay between T. vaginalis infection and neutrophil dynamics within pregnancy\'s immunological context provides valuable insights into potential therapeutic targets. This review advocates for further research aiming to enhance our understanding of neutrophil-parasite interactions and develop targeted interventions to ameliorate adverse outcomes associated with T. vaginalis infection in pregnant women.

Co-infection with HIV and malaria presents a multifaceted clinical scenario with intricate immunological interplays, wherein neutrophils, the primary mediators of innate immunity, emerge as pivotal actors. This paper aims to comprehensively analyze the dynamic role of neutrophils in the progression of HIV within the context of malaria co-infection. Neutrophils, conventionally viewed as short-lived effectors, exhibit remarkable plasticity and multifunctionality, contributing significantly to immune responses during co-infections. Their phenotype and functions undergo profound alterations in response to the complex milieu of both HIV and malaria, impacting disease progression and immunomodulation. This paper scrutinizes the nuanced alterations in neutrophil phenotypes, their diverse effector functions, and their contributions to immunopathogenesis within the HIV-malaria co-infection paradigm. Neutrophils, driven by dysregulated cytokines and inflammatory cues, exhibit heightened activation, potentially exacerbating tissue damage and chronic immune activation. Insights gleaned from understanding neutrophil dynamics in this co-infection scenario hold significant therapeutic implications. Potential interventions targeting neutrophil responses offer promising avenues for modulating immune dysregulation and managing disease progression. The review underscores the need for innovative therapeutic approaches aimed at harnessing neutrophil functionalities to mitigate HIV progression within malaria co-infected individuals. In conclusion, unraveling the intricate roles of neutrophils provides critical insights into the immunopathogenesis of HIV within the context of malaria co-infection. This comprehensive understanding not only sheds light on immune modulation but also presents a foundation for future therapeutic strategies aimed at improving clinical outcomes in this complex co-infection scenario.