Biofilm-related infections substantially contribute to bacterial
illnesses, with estimates indicating that at least 80% of such diseases
are linked to biofilms. Biofilms exhibit unique metabolic patterns that
set them apart from their planktonic counterparts, resulting in
significant metabolic reprogramming during biofilm formation.
Differential glycolytic enzymes suggest that central metabolic processes
are markedly different in biofilms and planktonic cells. The glycolytic
enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is highly
expressed in Staphylococcus aureus biofilm progenitors, indicating that
changes in glycolysis activity play a role in biofilm development.
Notably, an important consideration is a correlation between elevated
cyclic di-guanylate monophosphate (c-di-GMP) activity and biofilm
formation in various bacteria. C-di-GMP plays a critical role in
maintaining the persistence of Pseudomonas aeruginosa biofilms by
regulating alginate production, a significant biofilm matrix component.
Furthermore, it has been demonstrated that S. aureus biofilm development
is initiated by several tricarboxylic acid (TCA) intermediates in a
FnbA-dependent manner. Finally, Glucose 6-phosphatase (G6P) boosts the
phosphorylation of histidine-containing protein (HPr) by increasing the
activity of HPr kinase, enhancing its interaction with CcpA, and
resulting in biofilm development through polysaccharide intercellular
adhesion (PIA) accumulation and icaADBC transcription. Therefore,
studying the metabolic changes associated with biofilm development is
crucial for understanding the complex mechanisms involved in biofilm
formation and identifying potential targets for intervention.
Accordingly, this review aims to provide a comprehensive overview of
recent advances in metabolomic profiling of biofilms, including emerging
trends, prevailing challenges, and the identification of potential
targets for anti-biofilm strategies.