aureuscan hijackC. amplified titers of specific anticommensal antibodies, we spotlight that profiling these antibodies in the pilosebaceous unit by LFIAs may provide a unique signature for monitoring acne vulgaris. Keywords:acne vulgaris, antibody,C. acnes,C. aurimucosum, lateral circulation immunoassays,S. aureus == Introduction == Human blood contains not only antibodies provoked by infections and vaccinations but also antibodies acquired by exposure to commensal bacteria (Zhao and Elson, 2018). While the anticommensal antibody repertoire has not been profiled in full, immunoglobulin G (IgG) in human blood with broad specificity to bacteria in the gastrointestinal tract has been detected (Castro-Dopico et al., 2019). These anticommensal antibodies have been documented to elicit proinflammatory activities by activation of fragment crystallizable (Fc) receptors on macrophages (Castro-Dopico et al., 2019). The serological lateral circulation immunoassays (LFIAs) have been frequently used to detect the circulating antibodies (Banerjee and Jaiswal, 2018), mainly generated by infections or vaccinations including coronavirus disease 2019 (COVID-19) vaccines against SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) (Ravi et al., 2020). However, LFIA has been widely used in detection of anticommensal antibodies in people with health or disease condition. Antibodies toCutibacterium acnes, a bacterium associated with pathogenesis of 1-Methyladenosine acne vulgaris, in human blood have been clearly detected (Wang et al., 2018). The human sebaceous pilosebaceous unit is commonly referred to as 1-Methyladenosine the seat of acne vulgaris and harbors a heterogeneous community of microorganisms, includingC. acnes,Staphylococcusspp., andCorynebacteriumspp. (Grice and Segre, 2011). For example,Corynebacterium aurimucosumis PKP4 often detected in sebaceous sites in humans (Blaskovich et al., 2019) and erythromycin-resistantStaphylococcus aureusin the comedones of acne vulgaris patients (Sitohang et al., 2019). While the pathophysiology of acne vulgaris remains unclear, many of the aforementioned microbial species have been widely associated with acne vulgaris. Features of acne vulgaris can be irregular patterns of composition and large quantity of bacteria, dominance of virulent 1-Methyladenosine bacterial subtypes, or genetic elements or metabolites of bacteria and host cell responses, including activation of receptors and secretion of antimicrobial peptides or inflammatory cytokines in the microbiome of acne vulgaris compared with healthy skin (Chen et al., 2021). Microbial composition results from the next-generation sequencing (NGS) platform for 16S ribosomal RNA (rRNA) gene analyses have revealed severe alterations in bacterial abundances, or dysbiotic microbiomes, in acne vulgaris. In comparing microbial profiles of healthy and acne patients, the relative large quantity ofC. acneswas comparable in healthy skin compared 1-Methyladenosine to acne lesions, but a higher large quantity ofCutibacterium granulosumwas found in healthy skin (Rajiv et al., 2013).C. acneshas been classified into phylogenetic clades IA-1, IA-2, IB-1, IB-2, IB-3, IC, II, and III (Fitz-Gibbon et al., 2013). Strains from clades IA-2 (mostly ribotypes 4 and 5), IB-1 (ribotype 8), and IC (ribotype 5) are closely associated with acne vulgaris, whereas clade II strains that include ribotypes 2 and 6 are often 1-Methyladenosine detected in healthy skin (Lee et al., 2019). Profiles of genetic elements and metabolites of bacteria in healthy skin and acne lesions are also different. The gene-encoding ChristieAtkinsonMunchPeterson (CAMP) factorscamp1,camp2, andcamp4, which contribute to hemolysis and inflammation, were found to be more abundantly expressed in acne lesions (ONeill and Gallo, 2018). ThegehAgene (PPA2105) encodingC. acneslipase can increase sebum concentrations of free palmitate, which plays an important role in lipotoxic inflammasome activation of macrophages (Legrand-Poels et al., 2014). The secretion of interleukin 1 (IL-1) via activation of Toll-like receptor 2 (TLR2) by ligands present onC. acnescan be detected in inflammatory acne vulgaris (Graham et al., 2004). It has been reported that the mRNA and protein.