On 2016 Sep 19, Gustav van Niekerk commented:

We (van Niekerk G, 2016) have recently argued that sickness associated anorexia (SAA) may represent a strategy to maintain high levels of autophagic flux on a systemic level systemically. (Also see van Niekerk G, 2016 for an evolutionary perspective).

An upregulation of autophagy during an infection may be critical for a number of reasons:

• Serum and AA starvation induce autophagy in macrophages and protect against TB infection (Gutierrez MG, 2004).

• We speculate that hepatic autophagy may play a critical role in clearing LPS and bacteria rom circulation.

• Pathogens entering a cell must quickly subvert host processes to prevent being degraded by autophagy. In this regard, up regulation of autophagic flux would confront pathogens with a narrower window of opportunity to modulate host machinery. Thus, autophagy enhance cell autonomous defence.

• Autophagy processes ribosomal components into antimicrobial peptides (Ponpuak M, 2010). Note that all nucleated cells have ribosomes and are capable of autophagy, this suggesting that autophagy may again enhance cell-autonomous defence.

• Autophagy is also involved in the non-canonical expression of epitopes on MHC II by non-professional antigen presenting cells such as adipocytes, muscle and endothelium cells.

Autophagy may also be important in cell survival. As an example, tissue ischemia, the release of biocidal agents from immune cells as well as the increase in misfolded proteins resulting from a febrile response may lead to the generation of toxic protein aggregates. Here, autophagy may promote cell survival by processing ‘overflow’ of damage proteins aggregates when proteasome pathway is overwhelmed.

Fasting-induced autophagy may thus promote host tolerance and resistance.

On 2016 Sep 19, Gustav van Niekerk commented:

We (van Niekerk G, 2016) have recently argued that sickness associated anorexia (SAA) may represent a strategy to maintain high levels of autophagic flux on a systemic level systemically. (Also see van Niekerk G, 2016 for an evolutionary perspective).

An upregulation of autophagy during an infection may be critical for a number of reasons:

• Serum and AA starvation induce autophagy in macrophages and protect against TB infection (Gutierrez MG, 2004).

• We speculate that hepatic autophagy may play a critical role in clearing LPS and bacteria rom circulation.

• Pathogens entering a cell must quickly subvert host processes to prevent being degraded by autophagy. In this regard, up regulation of autophagic flux would confront pathogens with a narrower window of opportunity to modulate host machinery. Thus, autophagy enhance cell autonomous defence.

• Autophagy processes ribosomal components into antimicrobial peptides (Ponpuak M, 2010). Note that all nucleated cells have ribosomes and are capable of autophagy, this suggesting that autophagy may again enhance cell-autonomous defence.

• Autophagy is also involved in the non-canonical expression of epitopes on MHC II by non-professional antigen presenting cells such as adipocytes, muscle and endothelium cells.

Autophagy may also be important in cell survival. As an example, tissue ischemia, the release of biocidal agents from immune cells as well as the increase in misfolded proteins resulting from a febrile response may lead to the generation of toxic protein aggregates. Here, autophagy may promote cell survival by processing ‘overflow’ of damage proteins aggregates when proteasome pathway is overwhelmed.

Fasting-induced autophagy may thus promote host tolerance and resistance.