International Journal of Medical Sciences and Pharma Research

N1 and N2 Neutrophils in Breast Cancer: Mechanisms, Clinical Relevance, and Therapeutic Potential

2025-01-19T01:08:20-05:00

Neutrophils are key components of the immune system and play a significant role in the tumour microenvironment (TME) of breast cancer. These cells can undergo polarization into two distinct phenotypes: N1 and N2 neutrophils. N1 neutrophils are typically associated with antitumor immunity, characterized by the production of pro-inflammatory cytokines and reactive oxygen species (ROS), which help inhibit tumour growth and metastasis. On the other hand, N2 neutrophils contribute to tumour progression by secreting immunosuppressive cytokines, promoting angiogenesis, and enhancing metastatic spread. The balance between these two phenotypes can have significant implications for cancer progression and treatment outcomes in breast cancer patients. The polarization of neutrophils is regulated by a complex network of cytokines, growth factors, and signalling pathways in the TME. Factors such as IL-12, IFN-γ, and GM-CSF promote N1 polarization, while IL-10, TGF-β, and VEGF are key drivers of N2 polarization. These pathways influence neutrophil recruitment, activation, and survival within the TME. Strategies targeting neutrophil polarization could offer new opportunities for breast cancer treatment, particularly for patients with aggressive or metastatic disease.

Keywords: N1 Neutrophils, N2 Neutrophils, Breast Cancer, Tumor Microenvironment, Immunotherapy

N1 and N2 Neutrophil Polarization in Breast Cancer: Predictive Value for Treatment Outcomes

2025-01-20T12:19:15-05:00

Neutrophils, the most abundant white blood cells in the immune system, play a crucial role in breast cancer progression through their ability to polarize into two distinct phenotypes: N1 and N2. N1 neutrophils are considered antitumor effector cells that promote immune responses and inhibit tumour growth, while N2 neutrophils support tumour progression by promoting inflammation, immune suppression, and metastasis. The balance between these two phenotypes within the tumour microenvironment (TME) can significantly influence breast cancer development and response to treatment. The polarization of neutrophils in the TME is influenced by various factors, including cytokines, growth factors, and interactions with other immune cells. N1 neutrophils exhibit pro-inflammatory and cytotoxic properties that help limit tumour growth, while N2 neutrophils contribute to an immunosuppressive microenvironment that facilitates cancer progression and therapy resistance. Studies suggest that an increased presence of N1 neutrophils correlates with improved prognosis and response to therapies, whereas a predominance of N2 neutrophils is often associated with poor treatment outcomes and increased metastatic potential. This review examines the mechanisms underlying neutrophil polarization and the implications of these phenotypes on treatment responses in breast cancer.

Keywords: N1 neutrophils, N2 neutrophils, neutrophil polarization, breast cancer, treatment outcomes

Risk of Opportunistic Infections in Sickle Cell Patients with HIV: A Review

2025-03-02T00:24:07-05:00

Sickle cell disease (SCD) and human immunodeficiency virus (HIV) are both associated with significant immune dysregulation, making co-infected individuals highly susceptible to opportunistic infections (OIs). SCD leads to functional asplenia, chronic inflammation, and impaired immune responses, while HIV progressively weakens the immune system through CD4+ T-cell depletion. The interaction between these two conditions exacerbates immune dysfunction, increasing the risk of severe and recurrent infections. Opportunistic infections in SCD-HIV co-infected patients include bacterial pathogens like Streptococcus pneumoniae and Mycobacterium tuberculosis, fungal infections such as Cryptococcus neoformans, viral infections like cytomegalovirus (CMV), and parasitic infections such as Toxoplasma gondii and Plasmodium falciparum. These infections can lead to severe complications, including life-threatening anemia, neurological impairments, and multi-organ failure. Early diagnosis, infection prevention through vaccination and prophylaxis, and appropriate antiretroviral therapy (ART) are critical in mitigating these risks.

Keywords: Sickle cell disease, HIV, opportunistic infections, immunocompromised, co-infection

Endothelial Dysfunction in HIV-Infected Sickle Cell Disease Patients: A Review

2025-03-02T00:34:23-05:00

Endothelial dysfunction is a significant complication in patients with both sickle cell disease (SCD) and human immunodeficiency virus (HIV) infection, contributing to increased morbidity and mortality. In SCD, chronic hemolysis leads to elevated levels of free hemoglobin and reactive oxygen species, resulting in decreased nitric oxide (NO) availability and impaired endothelial function. Concurrently, HIV infection is characterized by persistent immune activation and inflammation, further exacerbating endothelial injury. The interplay between these two conditions creates a synergistic effect that heightens the risk of thrombotic events, cardiovascular disease, and organ damage. This review aims to elucidate the molecular mechanisms underlying endothelial dysfunction in SCD-HIV co-infected patients, focusing on the roles of oxidative stress, inflammatory cytokines, and the upregulation of endothelial adhesion molecules. We also examine the contributions of dysregulated coagulation pathways to the vascular complications observed in this population. Understanding these mechanisms is crucial for developing effective therapeutic strategies to mitigate endothelial dysfunction and improve patient outcomes.

Keywords: Endothelial dysfunction, Sickle cell disease, HIV infection, Vascular inflammation, Nitric oxide