@raney...sorry...here is the excerpt that I found most relevant to our situations with the lung:

N-acetyl-cysteine (NAC) is included in the World Health Organization’s list of essential medicines; a list that details the most relevant medications needed for a basic health system [1]. Acetyl-cysteine is a derivative of cysteine in which an acetyl group is attached to nitrogen. Due to its disulfide reducing activity, NAC is used as a mucolytic agent to promote expectoration [2]. NAC is commonly prescribed as an adjunct therapy in patients with a wide range of respiratory diseases characterized by formation of thick mucus, such as cystic fibrosis [2–4]. At high doses, NAC results in significantly improved small airway function and decreased exacerbation frequency in patients with stable chronic obstructive pulmonary disease (COPD) [3, 4]. NAC’s mucolytic activity is also the basis of its use in liquefying sputum samples for the microscopic detection of acid-fast bacilli (AFB) in suspected pulmonary tuberculosis (TB) patients [5]. Furthermore, in both experimental animal models and clinical studies, NAC displays a protective effect on acute liver injury induced by anti-TB drugs in acetaminophen-dependent or independent conditions [6–11]. In patients with type 2 diabetes, NAC holds promise in primary prevention of cardiovascular complications and systemic inflammation [12–14].

In addition to the above clinical applications, NAC has been employed as a potent anti-oxidant in several experimental models of infection and cancer in vitro and in vivo [15–20]. In these settings, NAC serves as a pro-drug to L-cysteine, which is a precursor to the biologic antioxidant glutathione. This anti-oxidant property of NAC is associated with strong anti-inflammatory effects, which have been suggested to inhibit the activation of nuclear factor-κB (NF-κB) with subsequent inhibition of cytokine synthesis [2, 21, 22]. In a mammalian model of Mycobacterium tuberculosis infection, NAC has been shown to diminish TB-driven lung pathology and inflammatory status, as well as to reduce mycobacterial infection loads in the lung [23]. These effects were attributed to the drug’s anti-oxidant properties and immune regulatory activities. Whether NAC limits M. tuberculosis infection in this situation through a direct microbicidal effect on M. tuberculosis was not addressed. Indeed, NAC has been shown to exhibit anti-microbial activity against a number of bacterial pathogens including Pseudomonas aeruginosa, Staphylococcus aureus, Helicobacter pylori, Klebsiella pneumoniae and Enterobacter cloacae [17, 24–26].

In this study, we demonstrate that NAC directly impairs the growth of several species of mycobacteria in vitro independent of its inhibitory effects on the host NADPH oxidase system. This anti-mycobacterial effect was also observed in an experimental model in vivo. Thus, NAC may limit M. tuberculosis infection and disease both through suppression of the host oxidative response and through direct antimicrobial activity. This dual host and pathogen directed function makes the drug an interesting candidate for use as adjunct therapy for tuberculosis.

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