There are two types of acne: inflammatory and non-inflammatory acne. To put it simply: non-inflammatory acne includes open and closed comedones (blackheads and whiteheads) and inflammatory acne, which occurs when the follicle wall ruptures, and includes papules, pustules and cysts and nodules (see here). Both types seem to share hyperkeratinisation and excessive sebum production. Non-inflammatory acne may also have P. acnes. But the main difference is that inflammatory acne has an obvious inflammatory/immune response, hence the pus
Remember the four main questions:
1. What are the causes of hyperkeratinisation of the hair follicle?
2. What are the causes of excessive sebum production?
3. If there is, is there any way to avoid colonisation by P. acnes?
4. What are the causes of the hyperinflammatory immune response?
The previous blog posts have focussed mainly on the first three questions. While resolving hyperkeratinisation and excessive sebum production may give one near immunity to acne (perhaps, not completely sure about that) they may not be attainable goals for some, in particular young males. Young males should have high levels of androgens, GH and IGF-1 and you wouldn’t want to change that. I wonder if some young males in hunter-gatherer tribes or traditional cultures had non-inflammatory acne
The Hyperinflammatory Immune Response
People with acne tend to have higher IL-1 levels  and an immune system primed for inflammation:
- People with acne are more sensitive to FFA, which are part of sebum and can come from P. acnes hydrolysing triglycerides 
- People with acne mount an immune response to P. acnes that isn’t seen in normal patients .
- People with inflammatory acne have neutrophils
that produce 43% more hydrogen peroxide than those with non-inflammatory acne
and controls (which seems dependent on gut bacteria as antibiotics largely
normalised hydrogen peroxidase generation) 
While I’ve portrayed inflammation as the last mechanism in inflammatory acne it may also initiate acne:
- Remember that those FFA that people with acne are more sensitive to, are comedogenic, irritate the follicular lining and can lead to rupture of the follicle wall, which releases the follicular contents into the surrounding dermis and leads to inflammatory lesions 
- It seems inflammation occurs prior to
hyperkeratinisation. IL-1 triggers
activation of keratinocytes  and elevated
IL-1α causes hypercornification and scaling (similar to initial events of
comedogenesis) to isolated follicle cells 
Acne and the Gut
A major cause of hyperinflammatory immune response likely originates in the gut as dysbiosis promotes a pro-inflammatory immune profile (high T helper cells, low T regulatory cells). People with acne are more likely to have GI related problems 
- Adolescents with acne are more likely to experience GI symptoms such as constipation, bad breath, and gastric reflux. Bloating was 37% more likely to be associated with acne
- Early research found 40% of those with have acne have low stomach acid (hypochloridia), which may promote SIBO and dysbiosis
- One measure of intestinal permeability found 66% of people with acne had intestinal permeability compared to none of the controls
- Another measure of intestinal permeability (reactivity to LPS) found 65% of people with acne reacted to LPS compared to no reaction from all the controls
- 54% of people with acne have altered gut
bacteria (one example is more Bacteroides, which are associated with stress)
Probiotics seem to reduce inflammation and oxidative stress and are to be therapeutic for acne: in one improving the standard treatment for acne and in another being more effective than antibiotics 
(1) The gut-skin connection: how altered gut function affects the skin
(2) Immune Dysfunction