This thesis delves into the complex interplay between host factors and microbiome composition,focusing on how host immune responses and social behaviors shape microbial communities. Initially, I employ a community ecology framework to model microbiota interactions, integrating host-mediated density dependence to assess the impact of immune strength on microbial dynamics. The findings reveal that while competitive communities remain stable under varying immune control strength, mutualistic communities are more susceptible to exogenous invasion under elevated host immune control, highlighting a trade-off in host defense strategies. Building on these theoretical insights, I analyze real-world cancer microbiome data to investigate the relationship between microbial community richness and abundance and host immune response. The analysis demonstrates that higher microbial richness and abundance correlate with increased mutualistic interactions and elevated expression of immune genes associated with poor stomach cancer prognosis. Conversely, communities with lower richness and abundance exhibit higher expression of antigen-presenting genes linked to improved survival, suggesting a more functional immune response. These results underscore the significance of both microbial diversity and abundance as biomarkers in disease outcomes. Lastly, I develop a social metacommunity model to examine microbiome transmission through host social networks. This model provides insights into how social interactions facilitate microbial dispersal among hosts, influencing community assembly. Collectively, this thesis integrates ecological principles with immunological and social factors to advance our understanding of host-microbiome interactions and their implications for health and disease.